Revise Notes General Sx Flashcards
Anal Fissure
Pathology
A tear in the lining of the anal canal - 90% occur in the posterior midline
Often occur as a complication of constipation
Defined as
Acute if < 6 weeks
Chronic if persist for > 6 weeks
Clinical Features
Severe pain in the anus which occurs during defaecation
May be associated with fresh red PR bleeding
Examination - small, wound/cut on anal mucosa, well-demarcated
Management
Treat constipation
Laxatives, adequate dietary fibre intake
Pain
Simple analgesia
If severe pain - topical anaesthetic (lidocaine 5%) - to be applied before defecation
Symptoms > 1 week without improvement
1st Line: Prescribe topical 0.4% GTN ointment BD for 6-8 weeks
SEs: headache in 1/4 patients
Unhealed anal fissure in child (> 2 weeks)
Refer to paeds
Unhealed anal fissure in adult (> 6-8 weeks)
If improvement with GTN - consider a second course of ointment, consider referral
If no significant improvement, options include:
Referral to colorectal team
Trial 2nd line treatment - topical diltiazem 2%
Secondary care
Surgical measures include:
Internal anal sphincter botox injections
Lateral sphincterotomy of internal anal sphincter muscle
Appendicitis
Pathophysiology
Inflammation of the appendix - most commonly arises as a result of luminal obstruction by a faecolith.
Obstruction allows proliferation of commensal microflora - the resultant inflammation causes increased pressure, resulting in ischaemia and if untreated necrosis & perforation.
Clinical features
Most common ages 10-30
Abdominal pain
Classically vague, central abdominal pain which subsequently migrates to the right iliac fossa
Nausea and vomiting, anorexia
Examination findings:
Abdominal pain, worst over McBurney’s point, with rebound and percussion tenderness
Rovsing’s sign - RIF pain on palpation of LIF
Psoas sign - RIF pain with extension of right hip
Imaging
US - often used 1st line to reduce radiation exposure (esp. children/pregnant patients)
CT abdomen - high sensitivity
Management
Laparoscopic appendicectomy - gold standard
Conservative Mx with antibiotics may be considered in high-risk surgical candidates - but has a high failure rate
Acute Mesenteric ischaemia
Pathology
Thrombus/embolism causes compromised arterial supply to bowel
Risk factors: Atrial fibrillation, smoker, vasculopath
Clinical features
Severe abdominal pain, out of proportion with clinical findings
Nausea and vomiting
Rectal bleeding
Examination findings: Non-specific, generalised tenderness, AF
Investigations
ABG - elevated lactate, metabolic acidosis
Triple phase CT scan (IV contrast)
Management
Emergency surgery, ABx, resuscitation
Chronic Mesenteric ischaemia
Pathology
A gradual compromise to arterial supply to bowel, due to atherosclerosis of coeliac trunk, MSA, IMA.
This results in postprandial ischaemic pain, as a consequence of increased oxygen requirement by bowel in the context of inadequate blood supply.
Risk factors: Vasculopath - smoking, DM, HTN, dyslipidemia, previous arterial disease (MI/stroke etc.)
Clinical features
The classic presentation is ischaemic, abdominal pain which occurs between 15 mins and 30 minutes after a meal, lasting for 30 mins to an hour.
Anorexia and associated weight loss
Investigations
CT angiography is the diagnostic modality of choice
Management
Medical measures - risk factor modification - smoking cessation, statin etc.
Surgical intervention - angiography with stenting is most common. Alternatives - bypass or endarterectomy.
Ischaemic colitis
Pathology
An acute compromise in the blood flow to the colon, which is less than its metabolic requirements, resulting in ischaemic injury.
Aetiology:
Systemic causes - septic shock, heart failure/cardiogenic shock
Thrombosis/embolism
Colonoscopy
Most commonly affects the splenic flexure
Clinical features
Acute-onset, colicky, cramping abdominal pain
Haematochezia / PR bleeding
Diarrhoea
Systemic upset - SIRS, pyrexia
Examination findings:
Abdominal distension
Tenderness over the affected segment of the colon
Generalised peritonism may suggest subsequent perforation
Investigations
CT is the investigation of choice
AXR shows thumb printing, mural thickening etc.
Management
Medical resuscitation may avoid the necessity of surgery
Surgical intervention should be considered if perforation, peritonitis etc.
Typically involves segmental resection, with colostomy formation.
Volvulus
Key learning
Pathophysiology: Rotation of gut on its mesentery, causing rapid strangulated intestinal obstruction.
Presentation:
Abdominal pain
Nausea/vomiting
Abdominal distension
Unable to pass flatus
AXR Findings:
Sigmoid volvulus ‘coffee bean’ sign
Caecal volvulus ‘embryo’ sign.
Management:
Fluid resuscitation, electrolyte replacement, NBM, flatus tube insertion, NG tube for decompression
Emergency laparotomy if needed.
Pathophysiology
Rotation of gut on its mesentery
Can result in rapid strangulated intestinal obstruction
Risk factors
Underlying intestinal malrotation (congenital)
Previous abdominal surgery (risk of adhesions)
GI malignancy
Presentation
Abdominal pain- may be local or generalised
Associated nausea/vomiting, distension, constipation
Absent or high pitched bowel sounds
May have features of peritonitis (guarding, rebound tenderness) if bowel ischaemia
Investigations
Bloods
Often electrolyte derangement
Imaging
Classical AXR signs (see below)
CT abdomen
Types
Sigmoid
Most common
Elderly constipated patients
Two loops of closely opposed dilated bowel (> 6cm)
AXR
‘coffee bean’ appearance (see below)
Management
Fluid resuscitation and electrolyte replacement
Flatus tube insertion to untwist volvulus
Keep NBM
NG tube for deompression and to aspirate if vomiting
Emergency laparotomy if above conservative management fails
Volcolus
Caecal
Congenital malrotation
May have ‘empty’ right iliac fossa as caecum displaced to left upper quadrant
AXR
‘embryo’ appearance- ectopically placed caecum, highly distended (>9cm)
Management
Fluid resuscitation and electrolyte replacement
Laparotomy to untwist
Complications
Large bowel obstruction
Peritonitis
Bowel perforation
Acute mesenteric ischaemia (rare)
UK National Cancer Screening Programmes
Key learning
UK National Cancer Screening Programmes:
Cervical Cancer:
Women aged 24.5-64.
Ages 25-49: Every 3 years; Ages 50-64: Every 5 years.
Screening via cervical smear and HPV test.
Abnormal results lead to cytology, colposcopy, and treatment or rescreening.
Breast Cancer:
Women aged 47-73, every 3 years.
Mammography for most, MRI for high-risk young women.
Triple assessment for abnormal results. DCIS treated as cancer.
Bowel Cancer:
Ages 60-74, every 2 years.
Faecal occult blood test (FOBT); abnormal results lead to colonoscopy.
Abdominal Aortic Aneurysm
Men aged 65 - ultrasound to measure abdominal aortic diameter
1) Cervical cancer screening
Offered to all women aged 24.5-64
25-49 screened every 3 years
50-64 every 5 years
Screened through cervical smear
Smear sent for HPV test
If positive -> cytological examination and cytology-> if abnormal-> colposcopy
Treat if cancer or rescreen at 1/3/5 years / repeat colposcopy depending on results
Poorest uptake in highest risk patients (low socio-economic background and high sexual activity)
Breast cancer screening
Offered to all women aged 47-73
Every 3 years
If over 70 can ask for screening through GP
Screening involves mammography
MRI can be used for young women at high risk due to family history
Separate high risk surveillance screening for those with known BRCA/TP53 mutations or strong family history
Breast cancer incidence has increased since screening due to high levels of detection of ductal carcinoma in-situ (DCIS)- treated as cancer but may not ever invade surrounding tissue
Screening Outcomes
If a breast cancer screening test is abnormal, the patient will undergo triple assessment of the breast
If triple assessment is normal, the patient will return to the normal screening programme
If cancer is detected (including DCIS) it will be treated
There is a 10% false negative rate
3) Bowel cancer screening
Offered to all aged 60-74
Every two years
If above 74 can request screening via GP
Screening via faecal occult blood test (FOBT)
If abnormal-> colonoscopy
If unclear-> repeat FOBT
If normal-> continue screening every 2 years
Colonoscopy:
Clear- return to screening
Cancer- treat
Polyp- removed and analysed and risk stratified:
Low risk- continue FOBT screening
Medium risk- Colonoscopy every 3 years
High risk- Colonoscopy in 12 months then 3 yearly
0.1% samples= cancer- majority confined to bowel
0.5%= polyps
Similarly to breast cancer there are also moderate/high risk surveillance groups- via regular OGD/colonoscopy
High risk groups:
First degree relative bowel cancer < 50
Familial adenomatous polyposis (FAP)
Hereditary non-polyposis colorectal cancer (HNPCC)
Inflammatory bowel disease (IBD)
Acromegaly
Abdominal Aortic Aneurysm screening
In the UK, the Abdominal Aortic Aneurysm (AAA) Screening Program targets men aged 65 and older. Screening is done using an ultrasound to measure the aortic diameter.
Diagnosis Threshold:
An aortic diameter ≥3 cm confirms an AAA.
Monitoring:
Small AAA (3.0–4.4 cm): Annual ultrasound surveillance.
Medium AAA (4.5–5.4 cm): Surveillance every 3 months.
Large AAA (≥5.5 cm): Consideration for elective surgery due to increased rupture risk.
Elective Surgical Management:
Surgery is recommended for large AAAs (≥5.5 cm) or if the aneurysm grows ≥1 cm per year. Options include open surgical repair or endovascular aneurysm repair (EVAR), with choice depending on patient suitability and risk assessment.
Other examples of regular screening:
Liver:
HCC: 6 monthly abdominal USS and AFP for all chronic liver disease patients
Variceal screening: Every 1-3 years for those with confirmed varices
Liver cirrhosis: Annual Fibroscan screening if Hep C, alcoholic liver disease, heavy drinkers
Cholangiocarcinoma: Annual USS and CA19-9 in all patients with primary sclerosing cholangitis
Renal:
Adult polycystic kidney disease: Regular US kidneys for relatives of patients
Diabetes (known diabetics):
Diabetic foot disease: annual screening
Diabetic retinopathy: annual screening
Genetic screening examples:
Cystic fibrosis: CFTR gene mutation
Haemochromatosis: HFE gene mutations
Cancer Screening Programme
Target Population
Screening Test
Frequency
Purpose
Breast Cancer Screening
Women aged 43-73
Mammography
Every 3 years
Early detection of breast cancer including DCIS
Cervical Cancer Screening
Women aged 25-64
Cervical smear
Every 3-5 years
Detection of abnormal cervical cells
Bowel Cancer Screening
Men and women aged 60-74
Faecal occult blood test (FOBT)
Every 2 years
Detection of blood in stool
Summary of UK National Cancer Screening Programme Sensitivity and Specificity
Cancer Screening Programme
Sensitivity
Specificity
Breast Cancer Screening
Approx. 80%
Approx. 90%
Cervical Cancer Screening
Approx. 80-90%
Approx. 90-95%
Bowel Cancer Screening
Approx. 60-70%
Approx. 90%
Bowel Obstruction
Definition
Mechanical/structural pathology results in physical obstruction to the contents of the bowel, with consequential dilatation of the proximal bowel.
Aetiology
Small bowel - hernias, adhesions (post-surgery), strictures (IBD)
Large bowel - colorectal cancer, volvulus, diverticular disease
Clinical features
The four cardinal signs of bowel obstruction:
Abdominal pain
Abdominal distension
Vomiting
Complete constipation
Examination findings: Distension, tenderness, tympanic percussion, classically ‘tinkling’ bowel sounds
Investigations
AXR - dilated bowel loops (3, 6, 9 rule) - key differentiating points between SBO and LBO include:
Small bowel
Dilated bowel > 3cm
Bowel loops have a more central position
Valvulae conniventes - lines traverse the whole bowel wall
Large bowel
Dilated bowel > 6cm, or > 9cm if caecum
Bowel loops have a more peripheral distribution
Haustra - indentations into the bowel wall - do not traverse whole bowel
Contrast-enhanced CT abdomen -
investigation of choice
Management
Management is dependent upon the cause
NG Tube insertion
IV fluid and electrolyte replacement
Conservative vs surgical management - urgent surgical intervention is indicated if there is evidence of intestinal ischaemia, or closed loop obstruction.
However in the absence of these, patients may be treated with a conservative ‘drip and suck’ regimen
Diverticular Disease
Pathophysiology
Diverticula are sac-like outpouchings of the bowel mucosa through the muscular wall occurring as a result of increased luminal pressure in the context of a weakened bowel wall.
The vast majority occur in the sigmoid colon.
Risk factors include: Obesity, age, low dietary fibre (and associated constipation)
Diverticulosis: The presence of asymptomatic diverticula
Diverticular disease: The presence of diverticula with associated symptoms (abdominal pain, altered bowel habit)
Diverticulitis: Inflammation of the diverticula, can be infective in aetiology
Acute Diverticulitis
Clinical Features
Severe lower abdominal pain - classically sharp pain, worst in the LIF
Systemic upset - malaise, pyrexia, tachycardia
PR bleeding
Features of complications - abscess, perforation - referred to as complicated diverticulitis
Imaging
1st Line: CT abdomen-pelvis - may demonstrate mural thickening of colon, pericolic fat stranding
Management
Admit if systemically very unwell/suspected complicated diverticulitis
PO Antibiotics: 1st Line (NICE): Co-amoxiclav 625mg TDS 5 days if managed in primary care
Pen. All. cefalexin 500mg TDS plus metronidazole 400mg TDS 5 days
Gallstones and Biliary Colic
Key learning
Gallstones form in the gallbladder due to bile imbalances and are often asymptomatic
Classically occur in middle aged overweight females
Biliary colic occurs due to gallbladder spasm against stone impacted in Hartmann’s pouch
Presents with severe intermittent RUQ pain worse after eating fatty food
No fever
Normal bloods
USS abdomen will show gallstones
Management includes pain relief and elective cholecystectomy
Gallstones
Pathophysiology
Gallstones are solid deposits that form in gallbladder
Form due to gallbladder hypomotility leading to stasis
3 main types:
Cholesterol- solitary, lighter and larger
Pigment- small, fragile, associated with haemolysis
Mixed- most common, made of cholesterol, often multiple
Epidemiology
Common- 15% prevalence
Risk factors
Female
Obesity
Middle aged (> 40)
Pregnancy
Diabetes
Smoking
Ileal disease
Family history
TPN use
Prolonged fasting
Clinical features
Often asymptomatic
Management
Asymptomatic stones in gallbladder do not need treatment
If in common bile duct consider surgical / endoscopic removal unless no symptoms for > 1 year
Biliary colic
Biliary colic
Pathophysiology
Gallbladder spasm against stone impacted in Hartmann’s pouch (neck of gallbladder)
Clinical features
Sudden onset RUQ pain
Colicky (intermittent) in nature
May radiate to shoulder blades/back
Worse following eating fatty foods
Pain resolves after a few hours
Associated nausea/vomiting
No fever
Investigations
Bloods normal including LFTs
US abdomen
Gallstones present
Management
Analgesia (opioids)
Rehydrate- IVI
NBM until symptoms resolve
Monitor for complications (see below)
Aim to discharge and plan for elective lap cholecystectomy
Complications
Obstructive jaundice
15% of those presenting with biliary colic have gallstones in CBD
These patients can develop obstructive jaundice
Management is either:
1) Surgery at time of lap chole
2) ERCP before or after lap chole
Gastrointestinal Perforation
Key learning
Often due to peptic ulcer disease, GI cancers, diverticulitis and appendicitis
Site of abdominal pain depends on site of perforation (i.e. RUQ in gallstones)
Assess for peritonitis (guarding, rebound tenderness, rigidity)
Erect CXR may show classical pneumoperitoneum
CT can localise lesion
Immediate management with IV fluid and antibiotics and urgent surgical intervention to repair perforation (usually via exploratory laparotomy)
Pathophysiology
Breach in the intestinal wall leading to spillage of contents into the abdomen
This causes peritonitis and systemic inflammation.
Management
Immediate:
Resuscitation with IV fluids and antibiotics
Definitive:
Surgical intervention- exploratory laparotomy and repair of the perforation.
Causes
Peptic ulcer disease
Gallstones
Appendicitis, diverticulitis, IBD
Bowel obstruction
GI malignancies
Trauma, foreign body, iatrogenic injuries i.e. previous surgery
Clinical Features
Symptoms
Sudden, severe abdominal pain
Location depends on site of perforation i.e. LLQ in diverticulitis vs epigastric in gastric ulcer
Associated nausea or vomiting, fever
Examination findings
Tenderness + peritonitism - guarding, rigidity, and rebound tenderness, reduced/absent bowel sounds
Investigations
Erect CXR- free air under the diaphragm (pneumoperitoneum)
CT can localise perforation
